Complications of fracture

 

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COMPLICATION OF FRACTURE HEALING

•  The most common complications of fracture healing are
  • Delayed Union
  • Nonunion
  • Malunion and osteomyelitis.  

COMPLICATION OF FRACTURE HEALING - DELAYED UNION

• In normal fractures, a certain amount of time is required before bone healing. This normal time may vary according to age, species, breed, bone involved, level of the fracture and associated soft tissue injury.
• So, delayed union refers to a fracture that has not healed in the usual time for that particular fracture. It occurs in any fractures.
  Causes

• The most common causes of delayed union are local factors
• Inadequate  fixation of the fracture fragments
• Inadequate blood supply
• Mal alignment of fracture fragments
• Interposition of soft tissues in the fracture site
• Bone loss
• Infection
• Some systemic factors also involve for delayed union like
• Heavy steroid doses
• The use of non steroidal anti-inflammatory drugs
• Starvation
• Advanced age
• Other metabolic disease

Diagnosis

• History-more time than normal healing time
• Radiographic examination
• The fracture line remains evident and characterized by feathery or wooly appearance and there is no sclerosis of the bone ends
• Evidence of osteogenic activity (callus) is visible but is minimal and may not bridge the fracture line.
• Uneven fracture surface
• Open medullary cavity

Treatment

• Line of treatment of delayed union is as follows
• Treatment is a prolonged period of appropriate immobilization
• If immobilization is not being used, it should be instituted
• If the method of fixation appears adequate, activity should be restricted and radiographs should be obtained after 4 weeks

Conclusion

• With adequate time and immobilization, most fractures unite.
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• When immobilization is inadequate and continues over a prolonged period, a delayed union becomes a nonunion.

COMPLICATION OF FRACTURE HEALING - NONUNION

• Nonunion refers to a fracture which is characterized by ceased or stopped of all evidence of osteogenic activity at the fracture site, movement is present at the fracture site and union is no longer possible without surgical intervention. Nonunion is common in diaphyseal fracture management in dogs and cats. Highest incidence of nonunion is found in radial bone and then in tibial bone.
  Radiographic fractures of nonunion

• Gap between fracture ends
• Closed medullar cavity
• Smooth fracture surfaces
• Sclerosis
• +/- hypertrophy or atrophy of bone ends

Classification of nonunion

• Nonunion is broadly classified into two groups: These two groups are further subdivided according to their cause and/ or radiographic appearance.
• Those that are biologically active ( or viable)
• Those that are biologically inactive ( or nonviable)
• Biologically active or viable nonunion

• This usually results from instability at the fracture site and characterized by a variable degree of proliferative bone reaction with interposed cartilage and fibrous tissue which is evidenced radiographically and histologically.  
• Hypertrophic or elephant foot nonunion: there is abundant callus formation but failure to bridge the fracture gap usually due to rotational instability.  
• Moderately hypertrophic or horse hoof nonunion: There is some callus formation but without bridging of the fracture gap.
• Oligotrophic nonunion: In this case there is no or very limited callus formation.   

• Biologically inactive or nonviable or nonreactive or avascular nonunion

• This type of nonunion fortunately is not common. Instability of fracture fragments is one of the major causes of this type.
• Dystrophic nonunion: One or both sides of the fracture line are poorly vascularised.
• Necrotic nonunion: If bone fragments are not “captured” by invading callus due to motion or more often infection, they may never become vascularised.
• Defect nonunion: Large fragments may be missing from open fractures, especially high energy gunshot fractures.   
• Atrophic nonunion: Fortunately this is rare in small animal orthopaedics. This is the end point of most nonviable nonunion with resorption and rounding of the bone ends with or without disuse osteoporosis.
  Diagnosis

• Diagnosis is based on relevant history, clinical and radiographic findings.

Treatment

• The aim of the treatment of nonunion is first to identify the cause and treatment of nonunion relies on the ability of the surge to reverse the etiology of the problem. Line to treatment as follows
• When a fracture is unstable, adequate stability must be provided
• When the nonunion lacks of osteogenic ability, autogenous cancellus bone should be added
• When the nonunion is avascular, vascularity is encouraged by adding an autogenous cancellus graft.

• Infected nonunion poses a challenging problem for the surgeon, however by combining the treatment plans of osteomyelitis and nonunion, the bone will heal. All dead and necrotic bone (sequesta) of nonunion site must be removed and the bone cultured for identification of organism and antibiotic sensitivity. Rigid internal fixation is provided and an autogenous cancellus graft is packed into the nonunion site.

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COMPLICATION OF FRACTURE HEALING - MALUNION

• Malunion is defined as a healing of the bones in an abnormal position or bones are allowed in a non functional anatomic position.
• Malunion can be classified as functional or non functional.
• Functional malunions are usually those that have small deviations from normal axes.
•  Malunion of long bones commonly results in degenerative arthritis of the joint above and below the malunion.
  Causes

• Fractures that were never treated
• Fractures in which the internal or external method of fixation was removed prematurely.

Treatment

• Correction of malunion is undertaken when the malunion is a functional liability to the animal.   
• Compartment syndrome: Severe swelling after a fracture can put so much pressure on the blood vessels that not enough blood can get to the muscles around the fracture.  
• Neurovascular injury: Some fractures are so severe that the arteries and nerves around the injury site are damaged.
• Infection: Open fractures can become infected when the jagged bone ends are exposed to the air where they have torn through the skin.
• Post-traumatic arthritis: Fractures that extend into the joints

HEALING OF TENDONS

• Three phases are recognized in the repair of tendon lacerations
  • an inflammatory phase,
  • a reparative (collagen-producing) phase and
  • remodeling phase.
• During the inflammatory phase (the first couple of days after injury), cells from extrinsic peritendinious tissue and/or intrinsic tissue from epitenon and endotenon invade the lacerated area.
• Many cells assume a phagocytic function. Other cells become fibroblasts, settle at the injury site and start to produce collagen (mostly type III) from approximately day 5 (reparative phase). Collagen is deposited in a random manner. Both cells and collagen fibrils are initially oriented perpendicular to the long axis of the tendon.
• During the remodeling phase (at approximately 2 months), type III collagen is replaced by type I collagen, collagen matures (cross-linking) and realignes itself parallel to the long axis of the tendon. During this phase, the tendon reduces the mass of scarr tissue and increases its tensile strength.
• It is thought that all tendons can heal both intrinsicly and extrinsicly, and that the contribution of each may depend on the type and site of tendon injury.
• For example, following lacerations within the tendon sheath, peritendinious structures (synovial sheath, periosteum, subcutaneous tissue, deep adventitia and fascia) provide most of the fibroblastic and vascular components. Although there is an intrinsic response, it is completely overwhelmed by the extrinsic response.
• In the absence of a synovial sheath, the intrinsic response plays a more significant role. Furthermore, there is also evidence that early mobilization may promote the intrinsic response, and consequently reduce scar formation and adhesions.
• Although our knowledge regarding tendon healing and repair has significantly increased during the last decades, tendon injuries are still a significant clinical problem, and complete functional recovery after tendon repair is rare
  • Tendon lacerations
  • Tendon dislocations
  • Tendon avulsions
  • Tendinitis/Tendinosis

TENDON LACERATIONS

• Tendon lacerations are usually associated with skin discontinuities. They are readily identified because of the abnormal range of motion of adjacent joint(s).
• Radiography and ultrasonography may be helpful in the further definition of the lesion.
• If the wound is fresh and clean with minimal tissue damage, primary repair is indicated.
• If the wound is contaminated or significant tissue damage is present, wound management and delayed tendon repair is recommended.
• Surgical repair with a modified Kessler (locking loop) or a triple pulley suture pattern, using non-absorbable suture material (Novafil ® ) is recommended.
• Aftercare consists of immobilization for 4-6 weeks, followed by a Robert Jones bandage for 7-10 days. The activity is then restricted for another 3-4 weeks.

TENDON DISLOCATIONS

• Four different tendon dislocations are recognized
  • Pectoral Limb (dislocation of the biceps tendon (rare))
  • Pelvic Limb (dislocation of the patellar tendon)
  • dislocation of the proximal tendon of the long digital extensor muscle
  • dislocation superficial digital flexor tendon (rare; most commonly seen in Shelties)
• Dislocation of the patellar tendon (patella luxation) is a very common disease. Patella luxations can be congenital or acquired, permanent or intermittent, and medially or laterally.
• In small dogs and toy breeds the luxation is congenital and usually in medial direction, while in larger breeds the luxation often is acquired and usually in lateral direction.
• If tendon dislocations are causing clinical problems, surgical treatment is indicated. Surgical treatment usually consists of reconstruction of the anatomical relationships. Both patella luxation and lateral luxation of the superficial digital flexor tendon are hereditary. 

TENDON AVULSIONS

• Tendon avulsions are usually the result of indirect MTU trauma and have a similar etiology as strain injuries.
• Examples of the Pectoral Limb are
• Avulsion of the biceps tendon (from scapula)
• Avulsion of the humeral head of the deep digital flexor tendons (from medial humeral epicondyle)
• Examples of avulsions of the Pelvic Limb are
• Avulsion of the gluteal muscles (from greater trochantor)
• Avulsion of the lateral or medial head of the gastrocnemius muscle (from distal femur)
• Avulsion of the gastrocnemius muscle (from the calcaneus)
• Avulsion of the long digital extensor tendon
• Four basic types of tendon - bone injuries occur
• separation of tendon from bone,
• avulsion of a small piece of bone with the tendon,
• avulsion fractures, and
• physeal fractures (in immature animals).

• Radiography and sonography may aid in the diagnosis of the lesion. Surgery is indicated for tendon - bone injuries. Severated tendons are reconstructed using non-absorbable suture material (i.e. Novafil) in a horizontal mattress, a Bunnel or modified Kessler suture pattern in the avulsed segment, which is then reattached to the bone by drill holes place at the site of the tendon insertion. If a small fragment of bone has been avulsed with a tendon, it can be either discarded or left with the tendon.
• The aftercare is as with tendon lacerations, and consists of immobilization for 4-6 weeks, followed by a Robert-Jones bandage for 7-10 days. Activity is then restricted for another 3-4 weeks.
• If the bone segment is large enough, the suture can pass through it or it can be secured with Kirschner wires or a small bone screw with or without spike washer.
• Most avulsion fractures in young dogs involve traction growth plates and are repaired using a tension band device or bone screw. Avulsion fractures involving the epiphysis are reattached with a bone screw with spike washer or treated as a tendon separation.

TENDINITIS/TENDINOSIS

• The etiology of tendinitis is very similar to the etiology of strain injuries. Just as strain injuries, tendinitis is an indirect injury is caused by stretching of the affected MTU, but now the pathology as located in the tendon. Furthermore, in several muscles both strain injuries and tendinitis have been diagnosed.
• Stretching of the tendon beyond the elastic limit results in plastic deformation, histologically characterized by loss of the collagen "wave-pattern" (crimp).
• At the molecular level, it is related to intrafibrillar sliding (within collagen fibers) beyond the elastic limit. If the process of disruption continues, tendon rupture may occur.
• Fortunately, with rest the initial lesions may heal, most likely via intrinsic repair processes. However, if healing is inadequate or if additional microtrauma is superimposed, tendinitis/tendinosis may result.
• Examples of tendon ruptures following indirect trauma are:
  • Pectoral Limb
    • Rupture of the biceps brachii tendon
  • Pelvic Limb
    • Rupture of the Achilles tendon
• Treatment of tendon ruptures following indirect trauma is as in tendon lacerations.
• Tendinitis is histologically characterized by fragmentation of collagen, edema with increased ground substance, separation of collagen and tenocytes, proliferation of small vessels, and mesenchymal tissue. There are no inflammatory changes within the tendon, thus tendinosis may be a more appropriate term. Inflammatory changes only become apparent following total tendon or major vascular disruption.
• Tendinitis is an uncommon diagnosis in small animals and in fact only recognized as a cause of lameness in the biceps brachii muscle (bicipital tendinitis). Clinical evidence of bicipital tendinitis is pain on deep palpation of the biceps tendon and pain or discomfort on flexion of the shoulder joint while the elbow is extended.
• Synovial analysis, radiography (arthrography), sonography and arthroscopy are recommended to confirm the diagnosis. Treatment consist of rest and anti-inflammatories. Surgical treatment consists of a tenotomy of the tendon alone (preferably arthro scopically) or tenotomy with reattached to the proximal humerus.
• Acute or chronic tendon trauma may also lead to dystrophic calcification of the affected tendon. Examples of tendon calcifications are
  • Dystrophic calcification of the biceps tendon
  • Dystrophic calcification of the infraspinatus tendon
  • Dystrophic calcification of the supraspinatus tendon
  • Dystrophic calcification of tendons may or may not be associated with active inflammation, and may or may not be associated with lameness. It is only considered as the cause of lameness if no other cause of lameness can be identified.
    Treatment may consist of rest, anti-inflammatories or if conservative treatment is unsuccessful surgical debridement, tenodesis or tendon release.